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The anti-inflammatory and anti-cancer properties of epigall
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PostPosted: Tue Oct 07, 2008 9:17 pm    Post subject: The anti-inflammatory and anti-cancer properties of epigall Reply with quote

Inflamm Res. 2008 Oct 2. [Epub ahead of print]

The anti-inflammatory and anti-cancer properties of epigallocatechin-3-
gallate are mediated by folate cycle disruption, adenosine release and
NF-kappaB suppression.

Navarro-Perán E, Cabezas-Herrera J, Sánchez-Del-Campo L, García-
Cánovas F, Rodríguez-López JN.

Departamento de Bioquímica y Biología Molecular A, Facultad de
Biología, Universidad de Murcia, E-30100, Espinardo, Murcia, Spain.

OBJECTIVE: To understand the mechanism by which (-)-epigallocatechin-3-
gallate (EGCG), the major polyphenol of green tea, exerts its anti-
inflammatory action. METHODS: To check our hypothesis that the anti-
inflammatory properties of EGCG could be related to its antifolate
action and whether adenosine and its receptors are involved in EGCG
action, we investigated the EGCG-induced suppression of NF-kappaB in
Caco-2 cell monolayer, which acted as a model of the human intestinal
epithelium. RESULTS: We demonstrate that the anti-inflammatory
properties of EGCG are associated with its antifolate activity. By
using a natural stable folate we were able to reverse the EGCG
suppression of TNF-alpha-induced NF-kappaB activation, the
phosphorylation and degradation of IkappaBalpha and the
phosphorylation of Akt in this human colon carcinoma cell line. These
suppressions were mediated by the release of adenosine following
disruption of the folate cycle by EGCG. By binding to its specific
receptors, adenosine can modulate the Akt and NF-kappaB pathway.
Moreover, EGCG produces a significant increase in a specific adenosine
receptor, which could explain the suppression of the constitutive
activation of NF-kappaB in colon cancer cells. CONCLUSIONS: The data
suggest that by modulating NF-kappaB activation, EGCG might not only
combat inflammation, but also cancer.

PMID: 18830563 [PubMed - as supplied by publisher]
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